ArticleCancer cell international2024
ANGPTL4 regulates ovarian cancer progression by activating the ERK1/2 pathway.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The role of ANGPTL4 in cancer: A meta-analysis of observational studies and multi-omics investigation.PloS one · 2025Pooled it
- Angiopoietin-like protein 4 deficiency promotes tumor immune infiltration and CD8Molecular therapy. Oncology · 2026Article
- Prenatal Exposure to PFOA Induces Ovarian Function Impairment via the Disruption of the PPARγ/ANGPTL4 Pathway.Environment & health (Washington, D.C.) · 2026Article
- Ex Vivo Microfluidic Model Identifies a Role for Shear Stress during Ovarian Tumor Cell Attachment to Peritoneal Mesothelial Cells.ACS biomaterials science & engineering · 2026Article
- ANGPTL4 suppresses progression and improves cisplatin sensitivity in cervical cancer.Scientific reports · 2025Article
- miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4.European journal of histochemistry : EJH · 2025Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease Induced by Microplastics: An Endpoint in the Liver-Eye Axis.International journal of molecular sciences · 2025Review
- Emerging roles of angiopoietin‑like 4 in human tumors (Review).International journal of oncology · 2025Review
- Transcription factors and hormone receptors: Sex‑specific targets for cancer therapy (Review).Oncology letters · 2025Review
- Transcriptome Analysis Suggests PKD3 Regulates Proliferative Glucose Metabolism, Calcium Homeostasis and Microtubule Dynamics After MEF Spontaneous Immortalization.International journal of molecular sciences · 2025Article
- Adipose Factor ANGPTL4: Its Role in Aging Mechanisms and Associated Diseases.Clinical interventions in aging · 2025Review
- Potential role of ANGPTL4 in cancer progression, metastasis, and metabolism: a brief review.BMB reports · 2024Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOvarian cancer (OC) has the highest mortality rate among all gynecological malignancies. A hypoxic microenvironment is a common feature of solid tumors, including ovarian cancer, and an important driving factor of tumor cell survival and chemo- and radiotherapy resistance. Previous research identified the hypoxia-associated gene angiopoietin-like 4 (ANGPTL4) as both a pro-angiogenic and pro-metastatic factor in tumors. Hence, this work aimed to further elucidate the contribution of ANGPTL4 to OC progression.
methodsThe expression of hypoxia-associated ANGPTL4 in human ovarian cancer was examined by bioinformatics analysis of TCGA and GEO datasets. The CIBERSORT tool was used to analyze the distribution of tumor-infiltrating immune cells in ovarian cancer cases in TCGA. The effect of ANGPTL4 silencing and overexpression on the proliferation and migration of OVCAR3 and A2780 OC cells was studied in vitro, using CCK-8, colony formation, and Transwell assays, and in vivo, through subcutaneous tumorigenesis assays in nude mice. GO enrichment analysis and WGCNA were performed to explore biological processes and genetic networks associated with ANGPTL4. The results obtained were corroborated in OC cells in vitro by western blotting.
resultsScreening of hypoxia-associated genes in OC-related TCGA and GEO datasets revealed a significant negative association between ANGPTL4 expression and patient survival. Based on CIBERSORT analysis, differential representation of 14 distinct tumor-infiltrating immune cell types was detected between low- and high-risk patient groups. Silencing of ANGPTL4 inhibited OVCAR3 and A2780 cell proliferation and migration in vitro and reduced the growth rate of xenografted OVCAR3 cells in vivo. Based on results from WGCNA and previous studies, western blot assays in cultured OC cells demonstrated that ANGPTL4 activates the Extracellular signal-related kinases 1 and 2 (ERK1/2) pathway and this results in upregulation of c-Myc, Cyclin D1, and MMP2 expression. Suggesting that the above mechanism mediates the pro-oncogenic actions of ANGPTL4T in OC, the pro-survival effects of ANGPTL4 were largely abolished upon inhibition of ERK1/2 signaling with PD98059.
conclusionsOur work suggests that the hypoxia-associated gene ANGPTL4 stimulates OC progression through activation of the ERK1/2 pathway. These findings may offer a new prospect for targeted therapies for the treatment of OC.
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